中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2012年
10期
748-750
,共3页
邹朝双%寇蕊蕊%高媛%谢克勤%宋福永
鄒朝雙%寇蕊蕊%高媛%謝剋勤%宋福永
추조쌍%구예예%고원%사극근%송복영
三邻甲苯磷酸酯%有机磷化合物诱发的迟发性神经病%自噬相关蛋白
三鄰甲苯燐痠酯%有機燐化閤物誘髮的遲髮性神經病%自噬相關蛋白
삼린갑분린산지%유궤린화합물유발적지발성신경병%자서상관단백
three-o-cresyl phosphate%Organophosphate-induced delayed neuropathy%Autophagy-related protein
目的 研究三邻甲苯磷酸酯(TOCP)诱导的迟发性神经病(OPIDN)中自噬相关蛋白Atg1、Atg5和Beclin1的变化,探讨OPIDN发生的分子机制.方法 取成年罗曼母鸡30只,随机分为对照组、1d、5d、10d和21d组(每组6只),对照组给予同体积的玉米油,各染毒组动物均按750 mg/kg经一次性灌胃染毒TOCP,分别在相应时间点处死动物取胫神经和脊髓,免疫印迹法检测胫神经和脊髓中Atg1、Atg5和Beclin1的相对含量.结果 与对照组相比,TOCP染毒后胫神经中Atg1含量1、5、10、21d分别下降了 29.8％、64.4％、43.5％和19.8％(P＜0.05)；TOCP染毒后Atg 5含量1、5、10、21d分别下降了36.8％、49.6％ 、51.2％和31.5％(P＜0.05);TOCP染毒后beclin1含量1、5、10天分别下降了 68.5％、66.3％和32.2％(P＜0.05).与对照组相比,TOCP染毒后脊髓组织中Atg1含量1、5、10d分别下降了23.5％、48.7％和20％(P＜0.05)；Atg5含量在TOCP染毒后1、5、10、21d分别下降了32.7％ 、51.5％、47.3％和39.6％(P＜0.05)；beclin1含量在TOCP染毒后1、5、10、21d分别下降了28.9％、50.2％、43.2％和28.3％(P＜0.05).结论 TOCP染毒干扰了母鸡神经组织中自噬相关蛋白的表达,可能与OPIDN的发病机制有关.
目的 研究三鄰甲苯燐痠酯(TOCP)誘導的遲髮性神經病(OPIDN)中自噬相關蛋白Atg1、Atg5和Beclin1的變化,探討OPIDN髮生的分子機製.方法 取成年囉曼母鷄30隻,隨機分為對照組、1d、5d、10d和21d組(每組6隻),對照組給予同體積的玉米油,各染毒組動物均按750 mg/kg經一次性灌胃染毒TOCP,分彆在相應時間點處死動物取脛神經和脊髓,免疫印跡法檢測脛神經和脊髓中Atg1、Atg5和Beclin1的相對含量.結果 與對照組相比,TOCP染毒後脛神經中Atg1含量1、5、10、21d分彆下降瞭 29.8％、64.4％、43.5％和19.8％(P＜0.05)；TOCP染毒後Atg 5含量1、5、10、21d分彆下降瞭36.8％、49.6％ 、51.2％和31.5％(P＜0.05);TOCP染毒後beclin1含量1、5、10天分彆下降瞭 68.5％、66.3％和32.2％(P＜0.05).與對照組相比,TOCP染毒後脊髓組織中Atg1含量1、5、10d分彆下降瞭23.5％、48.7％和20％(P＜0.05)；Atg5含量在TOCP染毒後1、5、10、21d分彆下降瞭32.7％ 、51.5％、47.3％和39.6％(P＜0.05)；beclin1含量在TOCP染毒後1、5、10、21d分彆下降瞭28.9％、50.2％、43.2％和28.3％(P＜0.05).結論 TOCP染毒榦擾瞭母鷄神經組織中自噬相關蛋白的錶達,可能與OPIDN的髮病機製有關.
목적 연구삼린갑분린산지(TOCP)유도적지발성신경병(OPIDN)중자서상관단백Atg1、Atg5화Beclin1적변화,탐토OPIDN발생적분자궤제.방법 취성년라만모계30지,수궤분위대조조、1d、5d、10d화21d조(매조6지),대조조급여동체적적옥미유,각염독조동물균안750 mg/kg경일차성관위염독TOCP,분별재상응시간점처사동물취경신경화척수,면역인적법검측경신경화척수중Atg1、Atg5화Beclin1적상대함량.결과 여대조조상비,TOCP염독후경신경중Atg1함량1、5、10、21d분별하강료 29.8％、64.4％、43.5％화19.8％(P＜0.05)；TOCP염독후Atg 5함량1、5、10、21d분별하강료36.8％、49.6％ 、51.2％화31.5％(P＜0.05);TOCP염독후beclin1함량1、5、10천분별하강료 68.5％、66.3％화32.2％(P＜0.05).여대조조상비,TOCP염독후척수조직중Atg1함량1、5、10d분별하강료23.5％、48.7％화20％(P＜0.05)；Atg5함량재TOCP염독후1、5、10、21d분별하강료32.7％ 、51.5％、47.3％화39.6％(P＜0.05)；beclin1함량재TOCP염독후1、5、10、21d분별하강료28.9％、50.2％、43.2％화28.3％(P＜0.05).결론 TOCP염독간우료모계신경조직중자서상관단백적표체,가능여OPIDN적발병궤제유관.
Objective To study the changes in the levels of autophagy-related proteins,Atg1,Atg5,and Beclin1,in organophosphate-induced delayed neuropathy (OPIDN) caused by tri-ortho-cresyl phosphate (TOCP),and to investigate the molecular pathogenic mechanism of OPIDN.Methods Thirty adult Roman hens were randomly and equally divided into control group and 1,5,10,and 21 d intoxication groups.Each hen in the intoxication group was administered TOCP by gavage at a single dose of 750 mg/kg,while each hen in the control group was administered the same volume of corn oil.The hens were killed at the corresponding time points,and their tibial nerves and spinal cords were collected.The levels of Atg1,Atg5,and Beclin1 in the tibial nerves and spinal cords were measured by immunoblotting.Results Compared with those in the control group,the levels of Atg1 in tibial nerves decreased by 29.8％,64.4％,43.5％,and 19.8％ at 1,5,10,and 21 d,respectively,after intoxication (P＜0.05); the levels of Atg5 in tibial nerves decreased by 36.8％,49.6％,51.2％,and 31.5％ at 1,5,10,and 21 d,respectively,after intoxication (P＜0.05); the levels of Beclin1 in tibial nerves decreased by 68.5％,66.3％,and 32.2％ at 1,5,and 10 d,respectively,after intoxication (P＜0.05).Compared with those in the control group,the levels of Atg1 in spinal cords decreased by 23.5％,48.7％,and 20％ at 1,5,and 10 d,respectively,after intoxication (P＜0.05); the levels of Atg5 in spinal cords decreased by 32.7％,51.5％,47.3％,and 39.6％ at 1,5,10,and 21 d,respectively,after intoxication (P＜0.05); the levels of Beclin1 in spinal cords decreased by 28.9％,50.2％,43.2％,and 28.3％ at 1,5,10,and 21 d,respectively,after intoxication (P＜0.05).Conclusion The intoxication of TOCP is associated with the significant changes in the levels of autophagy-related proteins in the nervous tissues of hens,which might be involved in the pathogenesis of OPIDN.
